Signs Of Hepatic Encephalopathy Research Articles

Infective Endocarditis Induced – Decompensation of Chronic Liver Disease Presenting as Hepatic Encephalopathy

Abstract Infective endocarditis (IE) occurs in people of older age, with artificial or damaged heart valves, immunocompromised states, and intravenous (IV) drug abusers as major risk factors. This case report describes a rare presentation of IE in a patient with chronic liver disease (CLD). A 38-year-old female with a history of decompensated CLD due to hepatitis C, presented with high-grade fever with chills, abdominal pain, shortness of breath, melena, and altered mental status. On examination, she had signs of hepatic encephalopathy and a systolic murmur in the aortic area. Imaging studies revealed an aortic valve vegetation with moderate aortic regurgitation, and blood cultures were negative. Treatment with meropenem and teicoplanin was started which resulted in clinical improvement. This case highlights the importance of considering IE in patients with CLD presenting with decompensation and suggests that early diagnosis and treatment are crucial in improving outcomes.

Giant hepatic hemangioma in a patient with cirrhosis: challenging to manage.

Giant hepatic hemangiomas are occasional in patients with cirrhosis. It remains a challenge to decide on the need for treatment and choose the most appropriate intervention. A 62-year-old woman was recently diagnosed with cirrhosis and complained of upper abdominal fullness, reduction in oral food intake, and weight loss of 6 kg over the last three years. Upper digestive endoscopy evidenced thin-caliber esophageal varices and significant extrinsic compression of the lesser gastric curvature. Abdominal computed tomography revealed an exophytic tumor in the left hepatic lobe, measuring 11.5 cm, which had progressive centripetal contrast enhancement from the arterial phase, compatible with hepatic hemangioma. Serum tumor markers were negative, and her liver function was unimpaired. The patient underwent surgical resection (non-anatomical hepatectomy of segments II and III) which had no immediate complications, and the histopathological evaluation confirmed cavernous hepatic hemangioma. Two weeks later, she was admitted to the emergency room with jaundice, signs of hepatic encephalopathy, and moderate ascites, and was further diagnosed with secondary bacterial peritonitis. As no perforations, abscesses, or fistulas were observed on subsequent imaging tests, clinical management was successfully carried out. This case highlights that giant hepatic hemangiomas may be symptomatic and warrant treatment. In the setting of cirrhosis and portal hypertension, physicians should be aware of the risk of hepatic decompensation following surgical resection, even in patients with Child-Pugh class A.

Mesoportal bypass surgery with congenital portocaval shunt in a child aged 1 year and 3 months

Introduction. Abernethy malformation (CEPS) is a rare condition in which portomesenteric blood bypasses the liver through a partial or complete shunt into the inferior vena cava. This pathology is extremely rare in children. Clinically, it can occur almost asymptomatically or under the guise of other diseases. It is manifested by signs of hepatic encephalopathy, pulmonary hypertension or hepatopulmonary syndrome. Mesoportal bypass surgery is an option for correcting portocaval shunts with the restoration of physiological blood flow in the liver.Since 2016, a center for treating developmental anomalies in the hepato-pancreato-biliary system in children has been operating in Filatov Municipal Children's Hospital (Moscow). To date, the center has performed more than 1,500 surgical interventions on the organs of biliopancreato-duodenal zone. For the period from 2016 to 2022, an endovascular occluder was used in 13 children with congenital portocaval shunts; surgical dressing – in 6 children.Description of clinical observation. This article describes a clinical case of a child with a congenital portocaval shunt. A comprehensive instrumental examination revealed a complete absence of portal blood flow in the liver of a newborn baby . The spleen vein and superior mesenteric vein flowed into the inferior vena cava as a single trunk. It is believed that liver transplantation is the only effective treatment for this type of pathology. Despite the ambiguous anatomy of liver vessels, the child was operated on for the mesoportal bypass. The architectonics of child's liver was restored, and he returned to an absolutely normal life without any life-threatening factors.Conclusion. This clinical case demonstrates the only described case of complete surgical cure of a complex liver vascular defect.

Jaundice and Weight Gain After Autologous Stem Cell Transplantation in a 28-Year-Old Patient With Diffuse Large B-Cell Lymphoma

Question: A 28-year-old white man with diffuse large B-cell lymphoma developed sudden weight gain and jaundice 2 weeks after autologous stem cell transplantation. The patient complained about abdominal pain and fatigue. He had no prior history of chronic liver disease or cholecystolithiasis but had initially displayed hepatic manifestation of lymphoma. On examination, he presented with an extended abdomen, leg edema, jaundice, and signs of hepatic encephalopathy. Lab results showed beginning liver failure with abrupt rise of liver enzymes (glutamate-oxaloacetate transaminase 3617 U/L, glutamate-pyruvate transaminase 1283 U/I) and hyperbilirubinemia (bilirubin 96.7 μmol/L) as well as deranged coagulation (international normalized ratio 2.5).

Detection of all-cause advanced hepatic fibrosis using an ensemble machine learning framework

The hallmark of liver injury is liver fibrosis. Ultimately, significant fibrosis deposition results in cirrhosis, whereby there are changes in liver architecture with nodule formation and ultimately, disturbances to liver function.1 Although the clinical features of liver decompensation are well described (ie, ascites, spider naevi, jaundice, signs of hepatic encephalopathy), patients who have early cirrhosis often have no clinical signs and might be entirely asymptomatic.2 The avoidance and prevention of liver fibrosis is one of the key objective for liver clinicians and is achieved through direct treatments such as antivirals, or through lifestyle modifications (eg, alcohol avoidance and weight loss).

ENDOTHELIUM DYSFUNCTION IN PATIENTS WITH LIVER CIRRHOSIS

Aim: To assess endothelial dysfunction in patients with liver cirrhosis. Material and methods: The study involved 95 patients with alcoholic liver cirrhosis. The data were subjected to analysis of variance involving the calculation of arithmetic mean value and variance (М±m), estimating the values validity according to Student’s t-test and measuring Pearson correlation coefficient for binary variables. Results: The brachial artery diameter was 0.4±0.02 mm narrower, with its blood velocity flow being 25.8±3.4 cm/s slower in the mean, in the patients with liver cirrhosis with signs of hepatic encephalopathy as compared to the control group. The maximum EDV values were recorded in the patients in Group I (7.5±1.9 %), while Group III patients displayed the lowest EDV value (5.6±1.9 %). The LC patients were found to exhibit a significant increase in the concentration of ET-1 up to 1.14±0.07 fmol/ml as opposed to 0.34±0.05 fmol/ml in the control group (р<0.01), an increase in the level of VWF by 139.4±24,8 % as compared to the control group (р<0.01) and D-dimer by a factor of 6.8. Conclusions: The patients with liver cirrhosis were found to have endothelial damage, namely the dysfunction of the vasoregulating activity of vascular wall against the background of portal hypertension. Changes in the vasoactive BAS values are indicative of the damage to the vascular endothelium in LC patients with signs of HE. A steady and gradual increase or decrease in the levels of ЕТ-1, VWF, АТ ІІІ, and D-dimer may suggest the progressive character of ED in the LC patients.

Congenital hepatic fibrosis (a case report)

Congenital hepatic fibrosis (CHF) is an autosomal recessive disorder of intrauterine morphogenesis of the portobiliary system, characterized by periportal fibrosis and defective remodeling of the bile ducts. The article describes the features of the clinical course, diagnosis and treatment of type I CHF in the different terms of a patient’s life: from birth to her pregnancy, during pregnancy and after childbirth. The aim of this work is to familiarize specialists with the problem of diagnosis and treatment of type I CHF in a patient with a provisional misdiagnosis of cryptogenic liver cirrhosis. Results. The features of type I CHF that determine a wider diagnostic testing in long-term unspecified liver pathology cases were identified. First-time decompensation of portal hypertension (PH) occurred at 35 weeks of gestation with the development of ascitic-edematous syndrome, hypersplenism, preeclampsia without signs of hepatic encephalopathy (HE). Cesarean section was performed at 37 weeks’ gestation and healthy baby was born. One year and 9 months after delivery, hypersplenism compensation was achieved by performing splenic artery embolization (SAE). There were no clinical manifestations of HE throughout the follow-up period. Conclusions. The diagnostic algorithm for a long-term compensated unspecified liver pathology with PH should confirm or rule out CHF. Type I CHF patients can give birth to a healthy child. SAE successfully compensates for hypersplenism and PH in type I CHF. Transient elastography is an effective method for the assessment of liver fibrosis progression in patients with type I CHF.

Hepatic encephalopathy: issues relevant to clinical practice

Hepatic encephalopathy (HE) remains one of the most serious complications of liver cirrhosis. Its clinical spectrum sometimes creates difficulties in the optimal diagnosis at the patient’s bedside and treatment. To present new data on the field of clinical management of cirrhotic patients with hepatic encephalopathy. The role of ammonia in the diagnosis of HE is still under discussion. In clinical practice, in patients with suspected overt HE, normal ammonia concentration can be used to exclude this diagnosis. In contrast, a high concentration of ammonia in the absence of clinical signs of HE should not serve as a criterion for this diagnosis and as a guide for treatment. A separate issue for discussion is the covert HE. The simplest and most affordable test for screening for covert HE and evaluating the effectiveness of therapy is the animal naming test, which can be done on bedside by physician or caregivers. Patients with covert HE need treatment that is similar in approach to overt HE. The diagnosis of overt HE and the methods of its therapy are well known. According to Russian recommendations, depending on the disease course in a certain patient, lactulose, rifaximin, L-ornithine L-aspartate can be used as first-line drugs, which is applicable to the treatment of both overt and latent PE. The main issues on the management of HE in liver cirrhosis relate to the diagnostic role of ammonia, optimal diagnosis and treatment strategy for covert HE, therapy of choice for both overt and latent HE. There are expert opinions and consensus documents on all these issues. Treatment of overt and latent PE is carried out according to the same principles. Drugs of choice: lactulose, rifaximin and L-Ornithine L-Aspartate.

Normalisation of the psychometric encephalopathy score within the Cameroonian population

BackgroundMinimal hepatic encephalopathy (MHE) is the presence of neuropsychological abnormalities detectable by psychometric tests. Psychometric Hepatic Encephalopathy Score (PHES) is a gold standard test for the early diagnosis of MHE in cirrhotic patients. The aim of this study was to standardize the PHES in a healthy Cameroonian population and to evaluate the prevalence of MHE among cirrhotic patients.MethodsThis was a prospective, multicentric study from 1 December 2018 to 31 July 2019 in two groups: healthy volunteers and cirrhotic patients without clinical signs of hepatic encephalopathy. The results of the number connection test-A, number connection test-B, serial dotting test, line tracing test were expressed in seconds and those of the digit symbol test in points.ResultsA total of 102 healthy volunteers (54 men, 48 women) and 50 cirrhotic patients (29 men, 31 women) were included. The mean age was 38.1 ± 12.55 years in healthy volunteers and 49.3 ± 15.6 years in cirrhotic patients. The mean years of education level was 11.63 ± 4.20 years in healthy volunteers and 9.62 ± 3.9 years in cirrhotic patients. The PHES of the healthy volunteer group was − 0.08 ± 1.28 and the cut-off between normal and pathological values was set at − 3 points. PHES of the cirrhotic patients was − 7.66 ± 5.62 points and significantly lower than that of volunteers (p < 0.001). Prevalence of MHE was 74% among cirrhotic patients. Age and education level were associated with MHE.ConclusionPHES cut-off value in Cameroonians is − 3, with MHE prevalence of 74% among cirrhotic patients.

Serum melatonin in dogs with congenital portosystemic shunting, with and without hepatic encephalopathy

BackgroundMelatonin is a hormone produced and secreted primarily by the pineal gland and mainly metabolised in the liver. Increased melatonin concentrations have been reported in human cirrhosis and hepatic encephalopathy...

Electroencephalogram Abnormalities in Very Young Children with Acute Hepatitis A Infection: A Cross-Sectional Study

Background: There is a shortage on studies concerned with electroencephalogram (EEG) abnormalities in neurologically asymptomatic children with acute hepatitis A virus (HAV) infection. Objectives: In the present study, we evaluated EEG patterns in HAV infected children who had no symptoms of overt or minimal hepatic encephalopathy (HE). Methods: Forty-five children infected with HAV infection along with 45 healthy children were studied. EEG was acquired in resting condition with closed eyes. Statistical analysis was performed in SPSS V. 19 software. Results: Abnormal EEG patterns were recorded in 16 (35.6%) children with HAV infection while no subject showed EEG abnormality in healthy subjects (P = 0.02). Irregular spike along with alpha wave was the most frequent pattern (13 out of 16, 81.2%). One patient (6.3%) showed delta wave, and two patients (12.5%) represented tri-phasic wave. The mean age of the patients with irregular EEG was significantly higher (89.6 ± 35.2 months) than patients with normal EEG (60.7 ± 36.2 months, P = 0.01). Although a considerable number of patients with abnormal EEG had abnormally high AST (15/16), and ALT (14/16) levels, the means of neither AST nor ALT were significantly different when comparing patients with normal (535.9 ± 571.8 and 660.1 ± 649.8 IU/L, respectively) and abnormal (666.4 ± 834.7 and 982.1 ± 1230.7 IU/L, respectively) EEG patterns. Conclusions: Abnormal EEG is a relatively common finding in children with acute HAV infection representing no signs of HE. Higher age and elevated hepatic enzymes levels may predict abnormal EEG patterns in these patients.

31-Year-Old Woman With Jaundice and Abdominal Pain

31-Year-Old Woman With Jaundice and Abdominal Pain

Short-Term Proton Pump Inhibitor Use and Hepatic Encephalopathy Risk in Patients with Decompensated Cirrhosis.

Objective: A window period of approximately 3–6 months is usually adopted in studies that evaluate hepatic encephalopathy (HE) risk in proton pump inhibitor (PPI) users. However, HE risk after short-term PPI exposure remains unclear. We explored the effect of short-term PPI exposure using a case-crossover study design. Design: Records of patients with decompensated cirrhosis who had received an HE diagnosis were retrieved from the National Health Insurance Research Database. PPI use rates were compared for case and control with window periods of 7, 14, and 28 days. The adjusted self-matched odds ratio (OR) and 95% confidence interval (CI) from a conditional logistic regression model were used to determine the association between PPI use and HE risk. Results: Overall, 13 195 patients were analyzed. The adjusted OR for HE risk after PPI exposure was 3.13 (95% CI = 2.33–4.20) for the 7-day window, 4.77 (95% CI = 3.81–5.98) for the 14-day window, and 5.60 (95% CI = 4.63–6.78) for the 28-day window. All PPI categories, except omeprazole and pantoprazole, were associated with an increased HE risk. Irrespective of other precipitating factors, such as recent gastrointestinal bleeding or infection, PPI significantly increased HE risk. Conclusion: Short-term PPI use is significantly associated with HE in patients with decompensated cirrhosis. Physicians should use PPI in these patients for appropriate indications, and carefully monitor signs of HE even after short-term exposure. Owing to the limitations of retrospective design in the current study, further study is warranted to confirm our findings.

Dietary management of liver disorders

The liver is responsible for many important functions, including metabolism of ingested nutrients and toxins, and production of plasma proteins, clotting factors and bile salts. When the liver is diseased or damaged, dietary therapy is beneficial in preventing further damage; supporting hepatic repair and liver function; and decreasing signs of hepatic encephalopathy. The nutritional status of patients with liver disease is often compromised by anorexia; nutrient malassimilation due to portal hypertension and cirrhosis; and decreased hepatic nutrient synthesis or storage capacity. Appetite and the amounts of protein, carbohydrates, fats, vitamins and minerals should all be considered. Previously, reduced dietary protein was often recommended; however, reducing dietary protein concentrations in all animals with liver disease is not appropriate. Nutraceuticals may have a beneficial effect in some cases. Nutritional support specifically for feline hepatic lipidosis, copper associated liver disease and hepatic encephalopathy are discussed.

Structural and functional abnormalities of vision-related brain regions in cirrhotic patients: a MRI study

PurposePrevious studies have focused on global cerebral alterations observed in cirrhosis. However, little was known about the specific abnormalities of vision-related brain regions in cirrhotic patients. In this study, we sought to explore neurological alterations of vision-related regions by measuring brain resting-state network connectivity, based on the structural investigation in cirrhotic patients without clinical sign of hepatic encephalopathy (HE).MethodsStructural and functional magnetic resonance image (MRI) data were collected from 20 hepatitis B virus (HBV)-related cirrhotic patients without clinical sign of HE and from 20 healthy controls (HC). Voxel-based morphometric (VBM) analysis and brain functional network analysis were performed to detect abnormalities in cerebral structure and function.ResultsCirrhotic patients showed regions with the most significant gray matter reduction primarily in vision-related brain regions, including the bilateral lingual gyri, left putamen, right fusiform gyrus, and right calcarine gyrus, and other significant gray matter reductions were distributed in bilateral hippocampus. Based on structural investigation focused on vision-related regions, brain functional network analysis revealed decreased functional connectivity between brain functional networks within vision-related regions (primary visual network (PVN), higher visual network (HVN), visuospatial network (VSN)) in the patient group compared with HC group.ConclusionThese results indicate that structural and functional impairment were evident in the vision-related brain regions in cirrhotic patients without clinical sign of hepatic encephalopathy. The physiopathology and clinical relevance of these changes could not be ascertained from the present study, which provided a basis for further evolution of the disease.

Incidence and risk factors for neurological signs after attenuation of single congenital portosystemic shunts in 253 dogs.

To determine the incidence, outcome, and risk factors for postattenuation neurological signs (PANS) and seizures after attenuation of single congenital portosystemic shunts (CPSS) in dogs. Retrospective cohort study. Dogs (N = 253) with single CPSS. Medical records of dogs treated by surgical attenuation of a single CPSS between February 2000 and July 2015 were reviewed for signalment and preoperative and postoperative clinical outcomes, including the occurrence of PANS. Univariable and multivariable binary logistic regression was used to assess risk factors for PANS and for seizures. Twenty-eight (11.1%) dogs developed PANS, including 12 (4.7%) dogs with seizures. Five (17.9%) dogs with PANS did not survive to discharge. Risk factors for PANS included the presence of hepatic encephalopathy (HE) immediately preoperatively (P = .038, odds ratio [OR] 2.704, CI 1.057-6.922) and increasing age (P < .001, OR 1.476, CI 1.223-1.780). Risk factors for seizures included the presence of HE immediately preoperatively (P = .048, OR 3.538, CI 1.013-12.363) and increasing age (P = .009, OR 1.364, CI 1.082-1.720). No association was found between the location of portosystemic shunts (extrahepatic and intrahepatic) and post-operative PANS (P = .532) or seizures (P = .620). Similarly, preemptive administration of levetiracetam did not influence the risk of PANS (P = .991) or seizures (P = .752). Preoperative HE and older age in dogs with a CPSS increased the odds of developing PANS and seizures in our population. Preemptive administration of levetiracetam did not protect dogs against the development of PANS or seizures. Surgical attenuation of a single CPSS should not be excessively delayed, and surgeons should stabilize the clinical signs of HE before surgery to prevent postoperative PANS and seizures.

Oral oxycodone/naloxone for pain control in cirrhosis: Observational study in patients with symptomatic metastatic hepatocellular carcinoma.

Pain management in cirrhosis is a clinical challenge. Most analgesics are metabolized in the liver and cirrhosis may deeply alter their concentration, favouring the appearance of side effects. We aimed to assess the efficacy and safety of oral prolonged-release association of oxycodone/naloxone tablets (OXN) in the treatment of moderate/severe cancer pain in cirrhotic patients with metastatic hepatocellular carcinoma (HCC). We enrolled n=32 HCC patients with moderate/severe cancer pain unresponsive to paracetamol alone or associated with codeine or tramadol. All patients received an initial OXN dose of 5mg bid to be gradually increased in case of insufficient analgesia. At baseline and follow-up visits, we evaluated: pain intensity (using the Numerical Rating Scale, NRS), patients' autonomy in daily activities (Barthel Functioning Index); bowel dysfunction (Bowel Function Index, BFI), signs of hepatic encephalopathy (HE) and other opioid-induced side effects. No clinically significant adverse effects were reported (median follow-up 122days). No significant worsening of the BFI score was noted and no cases of HE were detected. Two patients (6.3%) discontinued treatment before T14 because of mild nausea and dizziness. The remaining n=30 patients were assessed for efficacy. Treatment led to a significant reduction in the mean of pain scores both at T14 (-37.1±16.3%, P<.001) and at T28 (-55.6±21.5%, P<.001); Barthel scores showed gradual and significant increase from T0 (81.6±13.0) to T14 (86.5±11.4, P=.001) and to T28 (88.3±13.6, P=.009). OXN may be considered a safe and effective option in the fragile population of cirrhotic patients.

Hepatic Encephalopathy in a Red-Tailed Boa (Boa Constrictor Imperator)

A 5-year-old female red-tailed boa (Boa constrictor imperator) was presented for abnormal neurologic behavior. Ultrasound examination revealed an enlarged liver, with rounded margins and hypoechoic areas. A complete snake virus polymerase chain reaction (PCR) profile was performed together with diagnostic blood testing. The snake virus PCR profile results were negative. Supportive treatment for the patient consisted of fluid therapy and nutritional support, supplemented with carnitine. Lactulose was administered orally every 24 hours. The snake died 3 weeks after the initial presentation. Histopathological examination of the liver showed extensive necrotic degeneration with hepatocytic centrilobular organization and cholestasis. Histopathology of the central nervous system (CNS) revealed a degenerative pattern of neurons, and a hyperplastic aspect of the microglial cells, morphologically similar to Alzheimer type II astrocytes. The postmortem examination results indicate that the neurological signs were a consequence of hepatic encephalopathy (HE). Reptiles with hepatic disease may show a wide variety of clinical signs. The last stage of liver diseases is often HE. Diagnostic procedures include hematology, serum/plasma biochemistry, echography, and biopsy. The prognosis for a patient that is presented with clinical signs of HE is guarded at best. Recommended treatment for reptile patients that are diagnosed with HE is fluid support and more specific hepatic therapeutic agents, including lactulose, silymarin, and carnitine.

Status epilepticus in patients with cirrhosis: How to avoid misdiagnosis in patients with hepatic encephalopathy

PurposeStatus epilepticus (SE) in patients with cirrhosis is a rare but serious situation. Diagnosis may be difficult in emergency presentation, especially when patients present with hepatic encephalopathy (HE). Misdiagnosis must be avoided since some anti-epileptic drugs aggravate HE. In this retrospective study, we therefore assessed the frequency of SE in patients with cirrhosis, evaluated the accuracy of diagnosis and determined rates of mortality. MethodWe reviewed data from all patients hospitalized from 2005 to 2013 in the Hepatology ICU for complications of cirrhosis with an initial diagnosis of SE. We attempted to reach a consensus decision on a possible diagnosis of SE in reviews of EEG traces and medical records by an expert electrophysiologist, a hepatologist and a neurologist. ResultsAn initial diagnosis of SE was made for 20 patients with cirrhosis. Critical review suggested that 15 of these patients were correctly diagnosed with true SE. However, initial diagnoses may have been mistaken for at least 3 patients, who presented clinical and electrical signs of HE without evidence for SE. Overall, we estimated a prevalence of 0.7% for SE in patients with cirrhosis (15 of 2010 patients admitted to our ICU) in our series. In-hospital mortality was of 73%. In the 12 months after the SE episode, mortality was 87%. ConclusionAs SE may be misdiagnosed in patients with cirrhosis, a joint review of the patients by neurologists and hepatologists could reduce errors in diagnosis.

Retrospective evaluation of acute liver failure in dogs (1995-2012): 49 cases.

To characterize the clinical presentation and outcome of dogs with acute liver failure (ALF). Retrospective case series from January 1995 to December 2012. University teaching hospital. Forty-nine dogs were diagnosed with ALF defined as the acute onset of clinical signs accompanied by serum hyperbilirubinemia and coagulopathy (prothrombin time >1.5 times the upper limit of the reference interval) with or without signs of hepatic encephalopathy. Medical records were retrospectively analyzed for clinical presentation, history, physical examination findings, clinicopathologic data, diagnostic imaging findings, hepatic histopathology, treatment, and outcome. Presenting signs included anorexia (28/49, 57%), vomiting (25/49, 51%), neurologic abnormalities (17/49, 35%), and polydipsia/polyuria (10/49, 20%). Neurologic impairment compatible with hepatic encephalopathy occurred at some point during hospitalization in 28/49 (57%) of dogs. Common clinicopathologic abnormalities on presentation other than hyperbilirubinemia and increased serum liver enzyme activity included thrombocytopenia (25/49, 51%), hypoalbuminemia (23/49, 46%), leukocytosis (17/49, 34%), anemia (14/49, 29%), hypokalemia (13/49, 27%), and hypoglycemia (10/49, 20%). The causes of ALF included neoplasia (13/49, 27%), presumptive leptosporosis (4/49, 8%), and ischemia (1/49, 2%). The remaining cases were idiopathic although 15 of these dogs had exposure to possible hepatotoxins. Common lesions in the 35/49 (71%) dogs that had hepatic histopathology were necrosis (19/39, 48%), lipidosis (16/39, 41%), vacuolar change (7/49, 14%), and inflammation (4/49, 8%). Complications included ascites (20/49, 41%), bleeding tendencies (14/49, 29%), pancreatitis (12/49, 24%), and acute tubular necrosis (11/49, 22%). Seven (14%) dogs survived to discharge. Survivors had higher alanine aminotransferase activity, and were more likely to maintain normal albumin concentrations and not develop clinical bleeding or ascites during hospitalization. Canine ALF is associated with multiple etiologies and a high mortality rate. Strategies to increase survival are urgently required.